Microvascular Flow and Reactivity in Patients Presenting in the Acute Phase of COVID-19.

An association between the presence of previous cardiovascular disease and adverse prognosis
has been demonstrated in patients with COVID-19 (coronavirus disease-19), presenting
increases of up to 5-10 times in mortality.

As an initial process, the SARS-CoV-2 virus, anchored in the transmembrane
angiotensin-converting enzyme 2 (ECA2), penetrates host cells, including endothelial cells,
pericytes and macrophages, in addition to type II pneumocytes.

Cellular invasion results in massive release of several pro-inflammatory cytokines ("cytokine
storm"), such as IL-1β, IFN-1 and IL-6, by the cells of the immune system. In turn, cytokines
increase the process of vascular inflammation and the expression of leukocyte-vascular
endothelium adhesion proteins, which results in endothelial activation accompanied by a
pro-coagulant and pro-adhesive phenotype - between leukocytes, platelets, red blood cells and
vascular endothelium - characteristic of the dysfunctional endothelium in the
microcirculation, which results in severe changes in the microvascular flow and, as a result,
in tissue perfusion.

It is also worth noting that the patients most vulnerable to the development of complications
are those with pre-existing endothelial dysfunction, associated with several risk factors
such as male gender and smoking, and comorbidities such as hypertension, diabetes and
obesity, all of which are associated with poor prognosis in COVID -19.

Considering that the intensity of systemic microvascular changes in patients in the acute
phase of COVID-19 could be related to disease progression and prognosis, the present
cross-sectional and observational study aims to investigate the presence of endothelial
dysfunction in these patients, also evaluating associations between the presence of
endothelial dysfunction and demographic, clinical and laboratory variables.